演題詳細

一般口演 / Oral Session

一般口演 107 (Oral Session 107) :ウイルス感染症/血球貪食症候群

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日程
2013年10月13日(日)
時間
15:00 - 16:00
会場
第14会場 / Room No.14 (札幌市教育文化会館 3F 研修室305)
座長・司会
森 慎一郎 (Shinichiro Mori):1
1:聖路加国際病院 血液腫瘍内科
 
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Clinicopathological analysis for bone marrow histiocytic hyperplasia with hemophagocytosis

演題番号 : OS-3-180

稲井 邦博 (Kunihiro Inai):1、法木 左近 (Sakon Noriki):2、岩崎 博道 (Hiromichi Iwasaki):3、上田 孝典 (Takanori Ueda):4、内木 宏延 (Hironobu Naiki):1

1:Div. Mol. Pathol., Dept. Pathol. Sci., Univ. Fukui, Japan、2:Div. Tumor Pathol., Dept. Pathol. Sci., Univ. Fukui, Japan、3:Div. Infect. Control, Univ. Fukui Hosp., Japan、4:Div. Hematol. Oncol., Dept. General. Med., Univ. Fukui, Japan

 

The excessive release of inflammatory cytokines occasionally induces life-threatening hemophagocytosis called hemophagocytic syndrome (HPS). A similar condition, histiocytic hyperplasia with hemophagocytosis (HHH), is often seen in bone marrow collected during autopsy, whereas the pathogenesis of HHH remains unclear. Therefore, we performed a clinicopathological analysis of HHH from 70 cadavers autopsied at the University of Fukui Hospital. HHH was detected in 29 of 70 autopsies and was significantly complicated with hematological diseases (p<0.001), sepsis (p<0.01) and other infections (p<0.05), DIC (p<0.05), and splenomegaly (p<0.05). Data from medical records indicated no significant changes, except for the minimum values of WBC counts (p<0.001) and platelet counts (p<0.001), in HHH patients as compared to non-HHH patients. The levels of inflammatory mediators including TNF-α, IL-6, IL-1β, IL-8 and IL-10 in HHH patients were significantly increased with high correlation coefficients. The HHH cytokine profiles were similar to the cytokine profiles for HPS, sepsis, and febrile neutropenia. Additionally, the ratio of IL-8 to IL-10 in HHH cases was significantly increased as compared to non-HHH cases (p<0.01). Multivariate risk factor analysis identified hematological diseases (odds ratio, 6.73) and sepsis (odds ratio, 5.40) as independent risk factors for HHH. These findings suggest that HHH preferentially developed under conditions of excessive inflammation, such as hemopathy and sepsis.

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